Perio Final Lec1 Part 1

7/27/2019 Perio Final Lec1 Part 1

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slidesThis lecture is include

ntroductionToday we start a new topic which is more related to the true

periodontal disease in terms of clinical application we know that what

etiology means ? " cause " and today's lecture is a fundamental one you

will need this information for your course out until you graduate and

maybe later on because we said maybe lecture that basically periodontal

disease is an inflammation of the periodontal tissue (gingiva , PDL , andso on .. ) the cause of this inflammation multi factorial but it is related

mainly to the present of microorganisms in the oral cavity , specific type

of MO or specific percentage of it that induce bury-inner - reaction that

cause PD destruction .

well being physical, mentalgeneral as a state of: is definedealth,social so its normally a balance between the body ability to defend itself

against the invading MO (mainly bacteria ,some viruses and some fungal

species) . when we have this balance there is No PD destruction but once

this balance is shifted to either right or left side we will have problem if

the bacterial population is stronger than the host defense disease take

place on the other hand if the body ability to fight bacteria is more than

needed what happen is body destruction and this is very prominent in

case of autoimmune disease or immune mediated disease .


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NOTEIt was found that most of the destruction of PD tissue is not caused by

bacteria ! it caused by the exaggerated response of the host against the

bacteria "the pattern of body defense against bacteria dose a lot of

collateral damage".

Soo health : is balance between host defense and bacterial population ,

disease imbalance HD,PP .

we have theses microorganisms in our oralQ:when

cavity?

**The human intrauterine fetus is sterile , but after passing through

birth canal , the fetus acquires vaginal and fecal microorganisms

some bacterial colonization maybe detected in the mouth of the fetus

within first hours after birth . maybe you note from microbiology

courses that some or most of the bacteria with in the oral cavity are

microflora (good bacteria )they defend our selfs & defend the oral

cavity against some worse bactaria ..**After tooth eruption , more complex micro flora is established , we

found that > 500 species of bacteria that live in the oral cavity some

researchers said than we have >1000 MO species including bacteria

and other species.

**After the age of 2 years , human micro flora is established which

generally lives in harmony with the body (commensal or beneficial) .

Mechanisums that involoved in removal of bactria from theoro-pharyngeal area :1- Swallowing, mastication and blowing the nose .2- Flow of different fluids (saliva, nasal, GCF,..) .3- Tongue and oral hygiene measures .4- Movement of cilia in nose and sinuses .5-High turnover of the oral epithelial cells ( to differentiate between

soft and hard tissue u know that enamel is a hard tissue ; there is no

turn over , this happens with the normal mucosa so that's why we have


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dental caries , imagine that enamel can slough away the super facial

layer that intact from bacteria will slough but fortunately this is not

happen :P and this make dentistry in high value ) .

So although the belief have changed from all type of bacteria to the group

of bacteria the role of bacteria is still the focus or intention and important

Old beliefaccumulation ofcumulativePeriodontal disease are caused by

all type of bacteria on tooth.

Current ,understanding

A small group of bacteria are the initiators for the

disease and most of tissue destruction caused by host

defense reaction to bacteria

Therefore

The central role of microorganism has always been ,

and is still recognized


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These microorganisms, mainly bacteria, populates the oral cavity in

biofilms called: Dental Plaque .Dental plaque is defined clinically as structured , resilient yellow-grayish

substance that adheres tenaciously to the intraoral hard surface .

.

Soft deposits starts as Materia Alba that forms the dental pellicle

immediately after tooth brush saliva covers newly clean teeth and we

know saliva is composed of glycoproteins so this chemical which can be

removed by just eating or mouthwash & if its lift for enough time whathappens it becomes thicker & more deposits attached to this small layer

to form what we call Materia Alba so these are basically soft deposits and

they dont have ascertain organization or structure so that its easily

removed by water spray and mouthwash they dont need toothbrush ,,,now if those deposits leave for enough period it start organize itself and

form the Dental plaque which cant be removed by water spray or

mouthwash mechanical removal has to take place ,,, and this plaque if it

lift for more time it will form dental calculuswhich is the topic in the

next lecture EnshAllah - .

So again we have Materia Alba (soft tissue can be removed by water

spray mouthwash and toothbrush less organized ) + time well form

dental plaque (more organized cant be removed by water spray mouth

wash but we can remove it mechanically by tooth brush ) ++ time well

form dental calculus (more organized calcified dental plaque one andcant be remove even by tooth brush ) .


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** Dental plaque is a type of biofilm and biofilm is the bacteria when

they are attached to the surface basically matrial to cover themselves to

change the environment & make it resistant to external forces also

become resistant to inter microorganisms so basically this biofilms is able

to attach to hard tissue and soft tissue ( gingival tissue ) ; but themechanism of attachment of bacteria is or facilitate attachment to hardtissue rather than soft tissue.

***free flouting bacteria in the oral cavity dont causing disease , it has

to be adhere to surface in order to coz disease ; once they are attached

they form a community of the bacteria , the coz of disease not singlebacteria the couse is the community , these bacteria which have the

ability to attach to a surface are called initial colonizer not all bacteria has

the ability to attach to the surface and those colonizer are basically not

disease causing bactiria ( not violent ) they secrete extracellular

material then secondry colonizers become and attached themselves and

these are the bad one (secondary colonizers ) ; they multibly and form

anew more complex community and cause disease .. and this is generally

how biofilme formed .

Plaque composition :

1- 70% of the plaque is composed of micro-organisms, mainlybacteria .

>500 species


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108 bacteria (in diseased crevice)

-bacterial species: mycoplasma, yeasts, protozoa , parasites

and viruses .

2- Extracellular matrix 30 % :*epithelial cells.

**macrophages .

***Leukocytes .

****embedded in a matrix .

e :alcification of dental plaqu1- supragingival (above the gingival margine )

Coronalrelated to calculus and caries.

Marginalrelated to gingivitis.

The supragingival is the mostly associated to gingivitis(inflammation

of the gingivalsoft tissue ) .

2-subgingival when the plaque when the plaque is accumulate andextend below gingival margin ; related to preiodontitise (the

inflammation of the periodontal complexmore sever) .

We can find bactria adher to the soft tissue (gingival ) hard tissue

(tooth ) or in between < look at the pic in the next page


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unattached 3- tissue attached1-tooth attached 2-

Dental plaque and biofilms

Biofilms is very important the beginning of infection is start by

forming biofilmes .

Where can we see biofilms :

1-pt with hemodialysis in the tubes that are used in this process

2-R.T infection .

3- U.T infection .

4-PD.

*** Biofilms are: matrix-enclosed bacterial populations adherent to eachother and / or to surfaces or interfaces .


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**** They are ecological communities that evolved to permit survival of

the community as a whole .

*** the most important information is the fluid filled channels in the inner mostlayer we have channels they are like tunnels under ground (subways ) , theseare very important to the bacteria to receive there nutrients (fluid filledchannels ) which supply the bacteria by its nutrient ,, and this well makeinnermost layer away from the surface this channels is away from the surfaceand when we use mouthwash it kill the bacteria at the surface but dont

reach to the inner most layer & it was found that the bacterial in the biofilmsis much more resistance to antimicrobial compared to bacteria on the outsurface . Ex ( if u make single bacterial culture in the microbiology lab u needfor example [x] of amoxicillin to kill it but if these bacteria are in the biofilmsthey needs [500x] amoxicillin to be killed )

Fluid filled channels


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This pic shows how the biofilms is formed and stastirritating the gingiva .


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Note :

in the supraginival mineralization the source of minerals is

saliva while in the supgigival the source of minerals is the

GCF .

dental plaque formation1- Formation of the pellicle .2- Initial bacterial adhesion and attachment3- Secondary Colonization4- Plaque Maturation

Intercellular Matrix 20 30 % of the plaquemass Organic and inorganic material from saliva,

GCF and bacterial products .

Organic Inorganic

-polysaccharide

-protiens

-glycoprotiens

-lipid

Ca , P and traces of Na , K , F

Primary source saliva


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1-Formation of the pellical : The initial phase of plaque formation . All surfaces of the oral cavity are coated with a glycoprotein pellicle . The pellicle comes from saliva, GCF, bacterial, and host tissue cell

products & debries .

The hydroxyapatite surface: -ve charged phosphate groups

Salivary and crevicular fluid macromolecules components : +vecharged .

They interact directly or indirectly Mechanisms involved the following forces:

.

Dental pellical is important to protect and lubricate tissue BUT

Also a substrate to which bacteria can attach and accumulate to form

dental plaque ..

Note eno dental pellicle it is not bacterial derivative its only salivary

matrial and sub tissue !

___________________________________________________________

2-initial adhesion of bacteria


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Within a few hours, bacteria are found on the dental pellicle (primarycolonizers) .

Mechanisms not fully understoodSuggested stages:

of bacteria to the surface

Initial (reversible) adhesion

AttachmentColonization and plaque formation

Initially, Gram positive, e.g. Actinomyces vicosus, Streptococcus

sanguis

*** The primary colonizers are

1- aerobics because they have capacity to use oxygen for there living and

u know that oxygen is presented in an aerobic environment its simple u ca

imagine the superfacial layer that is exposed to the O2 is have to be

aerobic but the areas in the tooth are away from O2 so they cant live so

that the secondary colonizers become anaerobic they dont need O2 forlive and this will make them worse gays

2- G+ bacteria have the ability to use sugar and saliva to get therenutrients again imagine the inner most layer is away from saliva sothey have to depend in something else other than sugars and saliva

so environment change from G+ to G- change also there nutrient .

At the End of this stage (bacterial adhesion ) :

Shift will occur from primary aerobic (G+) colonizers to

secondary anaerobic (G-) colonizers .


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secondary colonizers-3

Primary colonizers cant cause disease by their own they need help from

other gays and those what we call secondary colonizers they start modifythe environment and they have lived in organized pattern they are co

aggregate in protein and bacterial biofilm and this create empty space for

other bactria to come and co aggregate .

Examples of these secondary colonizers : Prevotella intermedia,

Prevotella loescheii, Capnocytophaga spp., Fusobacterium nucleatum andPorphyromonas gingivalis .

4-blaque formation and maturation

A- Co aggregation ; (just understanding )ex if I belong to Al-shmary family any gay who is related to the

Al.shamry area is welcome by me so here in bactira colonize we see :

F. nucleatum with S. sangius .

P. loescheii with A. viscosus .Capnocytophaga ochracea with A. viscosus .

F. nucleatum with P. gingivalis

F. nucleatum with Treponema denticola .


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** look here streptococcus actinomyces produce lactate and formate by

metabolism lactate is used by veillonella which produce many mineral

used by prophyromonas gingivalis and so on .. so this is interactive

community of bacteria that make them able to live tolerant (Agonistinteraction see later *)

B- adhesionAdhesion start by which the bacteria start to attach themselves to

other bacteria on the surface and its suggested that this Bactria have

adhesive function .


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Streptococcus species are the most predominant pellicle colonizers and

provide an array of adhesins after attachment .

.

microbial interreaction

Agonistic

Interactions

Cooper

ation in

the

metabol

ism of

digested

proteins

Providi

ng

growth

factors

Providin

g

favorabl

egrowth

conditions

Inhibition

ofgrowth:

Competitio

n on

nutrients

Inhibition

of

attachme

nt

Antagonistic

Interactions


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In the pic above you can see 'corncob ' configuration : growth of cocci

on the surface of filamentous microorganisms .

here you see

test tube brushes are gram negative filamentous bacteria, some of

which may be flagellated .

long filaments held together by an amorphous extracellular matrix .

Subgingival ______ away from O2 _____ better environment to danger

bacteria _____ provide more than one surface to bactria ( hard & soft

tissue and in between ) .

Subgingival niches :

The tooth (or implant) surface

.

Subgingival plaque


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Subgingival bacteria have the capacity to invade dentinal tubules

plaque occurs during

pregnancy.

levels

intermedia proportions

ensitive

indicator of altered systemic hormonal situation than clinicalparameters of gingivitis.

Plaque as a whole is the important factor!

* non specific means any type of bacteria cause dieses , but it has been

found that this is not the case

it is seen that:

develope destructive periodontitis .

odontitis have affected sites next to

unaffected sites .

These findings indicate that not all plaque is equally pathogenic .

Non specific plaque hypothesis 1890

Spasific plaque hypothsis 1979


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.

depends on the presence of or increase in specific

microorganisms .

link with localized aggressive periodontitis .

Disease can be attributed to changes in the environment which disrupthomeostasis between the plaque microflora and host .

to periodontal disease , we need to have a susceptible host to have a

disease .

*** how dose plaque grow ?!!

In the past, it was thought that plaque grows by apposition of new

bacteria at the plaque surface .

division of adherent bacteria .

Clinical aspects of plaque formation

Topography of supragingival plaque

then supgingval

formation take place .

Ecology plaque hypothesis 1991


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. ex enamel is more smooth than cementom if

there is gingival recession is easier to bacteria to colonize

.

.

.

ttability of tooth surface is another factor .

Variation within dentition - more on:

.

.

.

.

.

not really!

& Thats it

Done by : zain salameen

Perio Final Lec1 Part 1

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